Abstract: Obesity is now recognized as one of the foremost modifiable cancer risk factors. Numerous, large-scale epidemiological studies have demonstrated that there is a clear association between the risk of cancer development at a number of sites and raised body mass index.
Despite an expanding body of epidemiological evidence in support of the link between obesity and cancer, the underlying molecular mechanisms responsible are poorly characterized.
Adipocytes from obese subjects exhibit an altered endocrine function and secretory profile leading to an increased release of proinflammatory molecules, resulting in a chronic low-grade inflammatory state that has been linked to the development of cancer.
The level of adipokine production from adipose tissue is strongly influenced by the immune cell populations present in adipose tissue.
Studies of circulating adipokine measurement are prone to bias, and although animal models have indicated some areas of promise, evidence from human studies is lacking.
Cross-talk between tumor cells and adjacent adipose tissue may be an important factor in the carcinogenic process.
Keywords: obesity, gastrointestinal cancer, adipokines, insulin resistance.